The capacity for metabolic heat production is a critical component of thermoregulation in the homeothermic newborn, because mechanism for heat conservation are poorly developed and because the surface/volume ratio is lage. The broad objective of this project is to invesigate the physiological stimuli and cellular mechanisms that regulate the perinatal development of aerobic metabolism. There are two specific aims for the coming year: First, the development of the ability to use milk fat as an energy source will be studied in neonatal rabbits. Several possible rate-limiting steps in tbe pathway for fatty acid oxidation will be considered including: fatty acylCoA synthetase, fatty acylcarnitine transferase, B-oxidation, and electron transport. Second, the development of mitochondrial respiratory function will be studied in neonatal rats. Within 2 hrs. of birth, the ATP plus ADP plus AMP content of the mitochondria increases 3-fold, and this has been shown to cause an increase in State 3 respiration. In the current year the mechanism by which the mitochondria are able to suddenly accumulate adenine nucleotides from the extramitochondrial space will be considered in detail.